Sensory-motor systems must be recalibrated to adapt to normally-occurring or pathologically-induced changes in the pattern of sensory inputs. For studies of this process, the key questions are pinpointing how the system is appraised of changes in its sensory inputs, and defining the mechanisms by which an adaptive response is generated. This highlights a general problem for excitable cells which is how to scale or vary their responses appropriately with changes in the quantity or pattern of their synaptic inputs. In many cases, critical changes in synaptic activity are communicated to neurons via N-methyl-D- aspartate (NMDA) or metabotropic (mGlu) type glutamate receptors. We propose to use a simple system--the electromotor system of electric fish, which controls the electric organ discharge (EOD)- -to study how alterations in sensory inflow can regulate the activity of motor output circuitry to adaptively change the circuit's and the animal's behavior. These alterations in the sensory inflow are processed in the CNS and ultimately communicated to the pacemaker neurons that control the EOD frequency via NMDA and, possibly, mGlu receptors. Activation of these receptors leads to long-term (many hours) adaptive changes in the firing frequency of these critical pacemaking neurons after the stimulus has ceased. In this proposal we wish to more fully characterize how sensory stimuli induce long-term shifts in motor output (EOD frequency) of behaving animals; identify in a slice preparation how activation of NMDA and mGlu receptors in pacemaking neurons could lead to long-term changes in their postsynaptic firing rates; and, finally, test the role of these receptors in controlling the behavior by blocking them in pacemaking neurons in a restrained behaving animal.